GLP-1 Glossary

Glycated hemoglobin — a blood test measuring average blood sugar over the past 2–3 months. Expressed as a percentage. Normal: below 5.7%. Pre-diabetes: 5.7–6.4%. Type 2 diabetes: 6.5% or above. GLP-1 medications reduce A1C by 1.5–2.3% depending on drug and dose.

The body's metabolic adaptation to weight loss — a reduction in resting calorie burn beyond what is expected from mass loss alone. A key cause of weight loss plateaus on GLP-1 therapy. Can reduce calorie expenditure by 200–400 calories/day. Counteracted by resistance training and adequate protein intake.

Body fat. Includes subcutaneous fat (under the skin) and visceral fat (around internal organs). Visceral fat is metabolically harmful and associated with cardiovascular disease, insulin resistance, and type 2 diabetes. GLP-1 medications preferentially reduce visceral fat.

A molecule that binds to a receptor and activates it, mimicking the effect of the natural ligand. GLP-1 medications are GLP-1 receptor agonists — they bind to and activate GLP-1 receptors throughout the body. Tirzepatide is a dual GIP/GLP-1 receptor agonist.

Insulin-producing cells in the pancreatic islets of Langerhans. In type 2 diabetes, beta cell function progressively declines over time. GLP-1 medications stimulate beta cells to produce insulin in a glucose-dependent manner and may have protective effects that slow beta cell decline.

A screening measure calculated from height and weight (kg/m²). Categories: Underweight <18.5, Normal 18.5–24.9, Overweight 25–29.9, Obese ≥30. Used to determine GLP-1 medication eligibility. Not a perfect measure of health but the current standard for treatment eligibility. Check eligibility with our BMI Calculator.

The most serious type of FDA drug warning — placed in a black box at the top of prescribing information. All GLP-1 medications carry a boxed warning for potential thyroid C-cell tumor risk (medullary thyroid carcinoma), based on animal studies. Human causality has not been established.

Progressive loss of kidney function, staged 1–5. GLP-1 medications can generally be used down to eGFR ≥15–30 mL/min depending on the drug. They have demonstrated renoprotective effects in clinical trials. Patients with CKD require closer monitoring as dehydration from vomiting can worsen kidney function.

A custom-prepared drug made by a licensed compounding pharmacy, not manufactured by the original drug company. Compounded semaglutide became common during the FDA-declared shortage (2022–2025). Quality, dosing accuracy, and sterility vary significantly. Only legal when sourced from FDA-registered 503B facilities.

A widely researched sports supplement with strong evidence for muscle preservation during caloric restriction. Recommended dose: 3–5g daily for people on GLP-1 therapy actively losing weight. Safe for healthy adults; discuss with doctor if you have kidney disease. Helps counteract lean mass loss on GLP-1 medications.

The structured process of gradually increasing a GLP-1 medication from a low starting dose to a therapeutic maintenance dose, typically over 12–20 weeks. Designed to allow GI tract adaptation and minimize nausea and vomiting. Never skip escalation steps — doing so significantly increases side effect severity.

A class of oral diabetes medications (sitagliptin/Januvia, saxagliptin/Onglyza) that work by blocking the enzyme DPP-4, which normally breaks down GLP-1. They increase endogenous GLP-1 levels modestly. Less potent than injectable GLP-1 agonists — produce 0.5–0.8% A1C reduction vs 1.5–2.3% for injectable GLP-1s.

A molecule that activates two different receptors simultaneously. Tirzepatide (Mounjaro/Zepbound) is a dual GIP/GLP-1 receptor agonist. This dual mechanism produces synergistically greater metabolic effects — more weight loss, better blood sugar control, and paradoxically less nausea than GLP-1-only agonists.

A measure of kidney filtration function, expressed in mL/min/1.73m². Normal: ≥60. CKD Stage 3: 30–59. Stage 4: 15–29. Stage 5 (kidney failure): <15. Relevant to GLP-1 therapy because dehydration from vomiting can reduce eGFR acutely, and some GLP-1 drugs require dose adjustment at low eGFR levels.

The first 12–20 weeks of GLP-1 therapy during which doses are increased stepwise. Weight loss is slower during this phase — the initiation doses are for tolerability, not full therapeutic effect. Most GI side effects occur during escalation and resolve once the maintenance dose is stable.

The colloquial term for the constant mental preoccupation with food — intrusive thoughts about eating, cravings, and food-seeking behavior — that many people with obesity experience. One of the most commonly reported effects of GLP-1 medications is a dramatic reduction in food noise, often described as "the chatter in my head about food just stopped."

An insurance plan's list of covered drugs. GLP-1 medications are typically placed on Tier 3–4 (specialty drugs), resulting in higher cost-sharing. Prior authorization is almost always required. Your drug must be on formulary for savings cards to apply. Check your specific plan's formulary before expecting coverage.

The rate at which food moves from the stomach into the small intestine. GLP-1 medications slow gastric emptying, which extends the feeling of fullness after meals and blunts post-meal blood sugar spikes. This slowing is also the cause of GLP-1-related nausea, vomiting, and the need to avoid large and fatty meals.

An incretin hormone secreted by K cells in the small intestine in response to food intake. Like GLP-1, it stimulates insulin secretion. Unlike GLP-1, it has direct effects on fat cells and appears to reduce GLP-1-induced nausea. Tirzepatide (Mounjaro/Zepbound) activates both GIP and GLP-1 receptors — this dual action is why it outperforms GLP-1-only drugs.

A natural incretin hormone produced by L cells in the gut after eating. It stimulates insulin secretion, suppresses glucagon, slows gastric emptying, and acts on the brain to reduce appetite. In type 2 diabetes, GLP-1 response is impaired. GLP-1 receptor agonist medications restore this signaling at therapeutic doses.

A hormone produced by pancreatic alpha cells that raises blood glucose by stimulating the liver to release stored glucose (glycogen). In type 2 diabetes, glucagon is often inappropriately elevated. GLP-1 medications suppress glucagon after meals, reducing fasting and post-meal blood glucose.

The time it takes for the concentration of a drug in the body to reduce by 50%. Semaglutide's half-life is ~7 days; tirzepatide's is ~5 days. This long half-life enables once-weekly dosing and means drug levels remain relatively stable between injections. Use our Half-Life Calculator to see your current drug level.

Abnormally low blood glucose (typically <70 mg/dL). Symptoms: shakiness, sweating, confusion, dizziness, rapid heartbeat. GLP-1 medications alone have very low hypoglycemia risk due to their glucose-dependent mechanism. Risk increases significantly when combined with insulin or sulfonylureas. Treat mild hypoglycemia with 15g of fast-acting carbohydrate (glucose tablets, juice).

Underactive thyroid — insufficient production of thyroid hormone. A commonly missed cause of GLP-1 non-response. Untreated hypothyroidism reduces metabolic rate and makes weight loss much more difficult. Check TSH levels before concluding you are a non-responder to GLP-1 therapy.

A class of gut hormones that stimulate insulin secretion in response to food intake. The two main incretins are GLP-1 and GIP. They account for 50–70% of post-meal insulin release in healthy people. GLP-1 medications are "incretin mimetics" — they mimic these hormones at pharmacological doses.

A condition in which cells don't respond normally to insulin, requiring the pancreas to produce more insulin to achieve the same blood glucose-lowering effect. The underlying driver of type 2 diabetes. Weight loss from GLP-1 therapy significantly improves insulin resistance, often allowing reduction in diabetes medications.

An essential amino acid and the primary trigger of muscle protein synthesis (mTOR signaling). The most important amino acid for muscle preservation during weight loss. Foods highest in leucine: whey protein, chicken breast, tuna, eggs, and dairy. This is why protein quality matters, not just quantity, on GLP-1 therapy.

A buildup of fibrous fatty tissue under the skin caused by repeated injections in the same spot. Reduces drug absorption and creates visible lumps. Prevented by systematic site rotation — never injecting in the exact same location twice in a row. See our Injection Site Guide.

A composite endpoint used in cardiovascular outcome trials, typically including non-fatal heart attack, non-fatal stroke, and cardiovascular death. Semaglutide (Wegovy) reduced MACE by 20% in the SELECT trial. This cardiovascular benefit was a major factor in GLP-1 medications becoming standard of care for high-risk patients.

The stable, long-term dose of a GLP-1 medication after completing the escalation phase. For Wegovy: 2.4mg/week. For Mounjaro/Zepbound: typically 5–15mg/week depending on response. You don't have to reach the maximum dose — the lowest dose that produces adequate weight loss and is well-tolerated is your ideal maintenance dose.

A rare type of thyroid cancer arising from C cells. Personal or family history of MTC is a contraindication to all GLP-1 medications due to the boxed warning. GLP-1 receptor activation in rodents caused dose-dependent C-cell tumors; this risk has not been confirmed in humans, but the contraindication remains firm.

The most commonly prescribed oral diabetes medication, typically the first-line treatment for type 2 diabetes. Reduces A1C by ~1–1.5%, is weight-neutral to slightly weight-reducing, and has some cardiovascular benefit data. GLP-1 medications are now preferred over or alongside metformin for high-risk patients per major diabetes guidelines.

Mechanistic Target of Rapamycin — a key cellular signaling pathway that regulates muscle protein synthesis. Activated by leucine-rich protein intake and mechanical stimulation (resistance training). The primary molecular mechanism through which adequate protein and exercise preserve muscle mass during caloric restriction on GLP-1 therapy.

A patient who loses less than 5% of body weight after 16+ weeks at a therapeutic GLP-1 dose despite consistent use. Affects approximately 10–15% of patients. Most apparent non-response has an identifiable cause — untreated thyroid disease, weight-promoting medications, or insufficient dose. True genetic non-response is rare.

A chronic disease characterized by excess body fat, typically defined as BMI ≥30. Associated with increased risk of type 2 diabetes, cardiovascular disease, sleep apnea, and many cancers. Recognized as a chronic disease (not a lifestyle choice) by the AMA since 2013. GLP-1 medications treat obesity as a chronic condition requiring long-term pharmacotherapy.

Prescribing a medication for a purpose, population, or dose not specifically approved by the FDA. Common and legal — physicians can legally prescribe any FDA-approved drug for any indication they consider medically appropriate. Ozempic and Mounjaro are frequently prescribed off-label for weight loss, even though Wegovy and Zepbound are the on-label weight-management versions.

Colloquial term for facial volume loss, hollowing, and skin sagging that can occur with rapid weight loss on GLP-1 medications. Not a direct drug effect — it is a consequence of rapid fat loss from the face. More common in older patients and those losing large amounts quickly. Not medically dangerous. Preventable with slower weight loss and adequate protein intake.

Inflammation of the pancreas — a rare but serious GLP-1 complication. Symptoms: sudden, severe abdominal pain radiating to the back, with nausea and vomiting. Risk is higher in patients with prior pancreatitis, gallstones, or heavy alcohol use. Stop GLP-1 therapy and seek emergency care if pancreatitis is suspected.

The study of how the body absorbs, distributes, metabolizes, and eliminates a drug over time. Key pharmacokinetic parameters for GLP-1 medications: half-life (semaglutide ~7 days, tirzepatide ~5 days), time to peak concentration (~24–72 hours post-injection), and time to full elimination (~5 half-lives).

A period of no weight loss despite consistent medication use, typically defined as 4+ weeks without change. Caused by adaptive thermogenesis, partial receptor adaptation, calorie creep, and muscle loss reducing metabolic rate. Addressable through protein optimization, resistance training, sleep improvement, and dose increases. Use our Plateau Calculator.

An insurance requirement that your doctor obtain approval before a drug is covered. Almost universally required for GLP-1 medications. Requires documentation of diagnosis, BMI, comorbidities, and clinical necessity. Denial rates are high on first submission; appeals and peer-to-peer reviews succeed frequently. See our Cost & Insurance Guide.

A drug that binds to a receptor and activates it, mimicking the action of the natural hormone. GLP-1 receptor agonists (semaglutide, liraglutide) activate GLP-1 receptors. Tirzepatide is a dual GIP/GLP-1 receptor agonist — it activates both receptor types simultaneously.

The brand name for oral semaglutide — the only oral GLP-1 medication currently available. FDA-approved for type 2 diabetes. Available in 3mg, 7mg, and 14mg daily doses. Must be taken on an empty stomach with a small amount of water, 30 minutes before any food or other medications. Less potent than injectable semaglutide for weight loss.

A condition combining high body fat with low muscle mass — associated with worse health outcomes than either obesity or sarcopenia alone. A key risk of GLP-1 therapy without proper protein intake and resistance training. Prevented by targeting 1.2–1.6g protein/kg/day and 2–3 resistance training sessions per week. See our Muscle Loss Guide.

The active ingredient in Ozempic (injectable, weekly, diabetes), Wegovy (injectable, weekly, weight management), and Rybelsus (oral, daily, diabetes). A GLP-1 receptor agonist with a ~7-day half-life, engineered with albumin-binding modifications that prevent rapid enzymatic degradation. The most prescribed GLP-1 medication globally.

A class of oral diabetes medications (empagliflozin/Jardiance, dapagliflozin/Farxiga) that lower blood sugar by causing glucose excretion in the urine. Reduce A1C by 0.5–1.0%, cause modest weight loss, and have proven cardiovascular and kidney benefits. Often used alongside GLP-1 medications in people with T2D and heart failure or CKD.

An insurance requirement to try one or more less expensive drugs before a more expensive drug is approved. Some plans require patients to fail metformin, a DPP-4 inhibitor, or another medication before approving a GLP-1. This can delay treatment by weeks or months. An appeal citing cardiovascular risk or other clinical urgency can bypass step therapy requirements.

An injection into the subcutaneous fat layer just under the skin — as opposed to intramuscular (into muscle) or intravenous (into a vein). All GLP-1 weekly pens are subcutaneous injections. Correct technique involves inserting at 90° into the fatty tissue of the abdomen, thigh, or upper arm.

The energy expended digesting and metabolizing food. Protein has the highest TEF at 20–30% (meaning 20–30% of protein calories are burned in processing). Fat: 0–3%. Carbohydrates: 5–10%. High protein intake on GLP-1 therapy therefore provides a modest but real metabolic advantage over high-fat or high-carbohydrate diets at the same calorie level.

The active ingredient in Mounjaro (diabetes) and Zepbound (weight management, sleep apnea). A dual GIP/GLP-1 receptor agonist with a ~5-day half-life. Produces greater weight loss (20–21% average at max dose) and better A1C reduction than semaglutide, with lower nausea rates. FDA-approved for diabetes May 2022; for weight management November 2023.

An informal term for tirzepatide — a single molecule that activates two incretin receptors (GIP and GLP-1) simultaneously. Coined to distinguish it from GLP-1-only agonists. The dual incretin mechanism is responsible for tirzepatide's superior efficacy compared to all previous GLP-1 class medications.

The body weight that the brain actively defends through hormonal and neurological mechanisms. GLP-1 medications effectively lower the set point by reducing appetite signaling, but when stopped, the body reverts to defending the original set point — explaining why ~66% of weight is regained after stopping. Long-term treatment is required to maintain the lower set point.